Background:Metabolic reprogramming is a hallmark of lung adenocarcinoma (LUAD) progression and therapy resistance, yet its clinical integration for prognosis and treatment remains limited. This study aimed to develop a metabolism-related prognostic score (MRPs) and investigate its biological, immunological, and therapeutic implications in LUAD. Methods:Transcriptomic and clinical data from TCGA and GEO were used to construct a prognostic model based on metabolism-associated genes via LASSO-Cox regression. The model was validated in internal and external cohorts. Functional enrichment, immune infiltration analysis, drug sensitivity prediction (TIDE), and single-cell RNA sequencing were performed. WARS2 was identified as a key gene and validated through qPCR, Western blot, immunohistochemistry, and functional assays in vitro and in vivo. Results:The MRPs model stratified LUAD patients into two subgroups with distinct prognoses. The high-risk MRP I subgroup showed enhanced oxidative phosphorylation, cell cycle activity, and protein synthesis, along with suppressed immune infiltration and lower immune scores. WARS2 was highly expressed in malignant epithelial cells and associated with proliferative and metabolic programs at both bulk and single-cell levels. WARS2-positive cells exhibited increased intercellular communication via adhesion-related pathways. Functional assays confirmed that WARS2 silencing impaired LUAD cell proliferation, invasion, and tumor growth. Conclusion:This study presents a novel MRPs system that captures LUAD metabolic and immune heterogeneity and surpasses traditional clinicopathologic parameters in prognostic performance. WARS2 emerges as a functional driver and therapeutic target. These findings offer a comprehensive framework for metabolic-state-based stratification and personalized treatment strategies in LUAD.

Non-small cell lung cancer (NSCLC) remains one of the leading causes of cancer-related mortality worldwide, and its response to immune checkpoint blockade is frequently limited by an immunosuppressive tumor microenvironment and insufficient innate immune activation. Here, we developed a biomimetic manganese-containing bimetallic metal-organic framework (MOF) nanosystem, termed PMOFM, for enhanced NSCLC immunotherapy through PRMT1 inhibition, cGAS-STING activation, and PD-L1 blockade. PMOFM was constructed by loading a PRMT1-selective inhibitor into a manganese-containing bimetallic MOF and coating the nanoparticle with an anti-PD-L1-conjugated macrophage membrane to confer tumor-targeting and immunoregulatory properties. PMOFM exhibited favorable physicochemical characteristics, colloidal stability, efficient drug loading, and enhanced tumor accumulation. Mechanistically, PMOFM relieved PRMT1-mediated suppression of cGAS, while Mn2⁺ release further enhanced cGAMP-STING signaling, resulting in increased cGAMP production, elevated cGAS and pSTING expression, and amplified downstream inflammatory responses. In both subcutaneous and orthotopic NSCLC mouse models, PMOFM achieved superior tumor suppression and significantly prolonged survival without evident systemic toxicity. Moreover, PMOFM markedly increased intratumoral IFN-β, CXCL10, TNF-α, IL-6, and IFN-γ levels and promoted CD4⁺ and CD8⁺ T-cell infiltration. Collectively, this study presents a biomimetic MOF-based nanoplatform that integrates innate immune priming with immune checkpoint blockade, providing a promising strategy for enhancing immunotherapy against NSCLC.

Cigarette smoke-mediated chronic pulmonary damage constitutes a critical predisposing factor for chronic obstructive pulmonary disease and lung cancer pathogenesis. Polydatin, a naturally occurring stilbenoid characterized by its potent anti-inflammatory and antioxidant properties, has yet to be fully elucidated regarding its protective role and the underlying molecular mechanisms in CSE-induced pulmonary injury. Cigarette smoke extract (CSE)-induced lung injury murine models and MLE12 cells were treated with polydatin or other conditions. The investigation encompassed both intravital and extracorporeal modalities. Evaluations included pulmonary index, histopathology, oxidative stress markers, transcriptomic sequencing, protein expression (AKT/FoxO3/Bim), apoptosis (TUNEL), intestinal metabolomics, 16S rRNA microbiota profiling, and immunohistochemical staining of colon tissue. The administration of polydatin dose-dependently in vivo alleviated CSE-induced systemic impairments including weight loss, pulmonary edema, and oxidative stress concurrently demonstrating high biocompatibility and low systemic toxicity. Furthermore, it modulates the intestinal microecology by depleting g__Pantoea and g__Enterococcus abundance, concurrently restoring mucosal barrier integrity via the enhancement of ZO-1 and Occludin levels. Mechanistic analysis demonstrated that polydatin directly interacts with AKT1 at the Thr308 residue, thereby reversing the CSE-induced attenuation of AKT1 and FoxO3 (Ser253) phosphorylation. This restoration facilitates the nuclear-to-cytoplasmic translocation of FoxO3 and subsequent downregulation of the pro-apoptotic protein Bim. This regulatory cascade effectively curtails apoptosis and DNA fragmentation, with a concomitant decrease in Bax and Cleaved-Caspase 3 expression. In conclusion, polydatin exerts suitable protective effects against CSE-induced pulmonary injury by attenuating apoptosis through the AKT-FoxO3-Bim signaling cascade and simultaneously orchestrating the gut microenvironment. These findings highlight the potential of polydatin as a promising natural therapeutic agent for lung disorders.

Esophageal cancer (ESCA) is a leading cause of cancer-related mortality in China, with over 95% of patients diagnosed at advanced stages, resulting in low survival rates. Early detection is critical for improving outcomes, yet current screening methods are invasive or lack sensitivity. We developed a non-invasive early-detection model by integrating circulating cell-free DNA (cfDNA) methylation and fragmentomics features. Using a three-layer stacked ensemble machine learning framework, we analyzed multicenter blood samples from 309 participants, including ESCA patients and high-risk individuals. The integrated model called ESim-seq (Esophageal Cancer Screening with Integrated Model) achieved an AUC of 0.994 (95% CI: 0.979–1.000) in validation. At 99% specificity, sensitivity reached 87.3%, with simulated screening showing a 24.8% increase in stage I detection. Stratified analyses confirmed robustness across demographics, risk factors, and tumor stages. Clinical benefit modeling projected a 56.3% stage I detection rate under ideal conditions, significantly improving survival outcomes compared to standard care. This study developed a cfDNA-based analytical framework and demonstrated the advantage of multi-feature integration for early detection of ESCA.

BACKGROUND:Esophageal cancer is the 11th most common malignancy and the 7th leading cause of cancer-related death globally. Identifying key molecules and underlying mechanisms in the progression of esophageal cancer represents an effective strategy for developing novel therapeutic approaches. METHODS:DDX18 expression in clinical specimens was evaluated by immunohistochemistry and western blot analysis. Functional assays were performed in cells with either DDX18 knockdown or overexpression. Dual luciferase reporter assays and chromatin immunoprecipitation (ChIP) were conducted to validate the interaction between YY1 and the DDX18 promoter. A xenograft tumor model was utilized to investigate the role of DDX18 in vivo in esophageal cancer. RESULTS:DDX18 was found to be markedly overexpressed in esophageal cancer, with its levels significantly higher in patients with pathological grade III compared to those with grades I-II. In vitro, DDX18 enhanced cell proliferation, migration, and invasion, while concurrently suppressing apoptosis. Furthermore, DDX18 promoted epithelial-mesenchymal transition (EMT) and activated the AKT/mTOR signaling pathway. The use of AKT inhibitors effectively abrogated the oncogenic effects of DDX18. Dual luciferase and ChIP assays confirmed that YY1 binds to and stimulates DDX18 transcription. In rescue experiments, YY1 countered the inhibitory effects of DDX18 knockdown on cell proliferation, EMT, and AKT/mTOR activation. In vivo, DDX18 knockdown resulted in reduced tumor growth. CONCLUSIONS:The transcription of DDX18 was activated by YY1, and DDX18 promoted tumor cell growth and EMT through the AKT/mTOR signaling pathway in esophageal cancer cells.

Cancer has become one of the major diseases threatening human health in the twenty-first century due to its incurability. In 2022, new cases of esophageal and gastrointestinal cancers accounted for 17.1

ObjectiveTo summarize the effect of the timing of lung transplantation and related treatment measures on clinical prognosis of patients with paraquat poisoning. MethodsClinical data of a patient with paraquat poisoning undergoing bilateral lung transplantation were retrospectively analyzed. Clinical manifestations, auxiliary examination, diagnosis and treatment of this patient were summarized and analyzed. ResultsA 17-year-old adolescent was admitted to our hospital due to nausea, vomiting, cough and systemic fatigue after oral intake of 20-30 mL of 25% paraquat. After symptomatic support treatment, the oxygen saturation was not improved, and pulmonary fibrosis continued to progress. Therefore, sequential bilateral lung transplantation was performed under extracorporeal membrane oxygenation (ECMO). After postoperative rehabilitation and active prevention and treatment for postoperative complications, the patient was discharged at postoperative 50 d. ConclusionThe timing of lung transplantation after paraquat poisoning could be selected when the liver and kidney function start to recover. Active and targeted prevention of potential pathogen infection in perioperative period and early rehabilitation training contribute to improving clinical prognosis of lung transplant recipients.

M2-type macrophages (M2 Phi) play a pro-tumorigenic role and are closely associated with tumor development, where metabolic dysregulation exacerbates the immunosuppressive tumor microenvironment and fosters tumor growth. Mitochondria serve as the regulatory center of cellular metabolism, yet effective methods to modulate M2 Phi mitochondria within the tumor microenvironment remain lacking. In this study, we developed a technique utilizing the bio-encapsulation of mitochondria in Zeolitic Imidazolate Framework-8 (ZiF-8), referred to as Mito@ZiF-8. Our findings demonstrated that this coating protects intact mitochondria and preserves their bioactivity over an extended period after isolation. We successfully delivered Mito@ZiF-8 into M2 Phi, which inhibited the secretion of pro-inflammatory factors, promoted the release of anti-inflammatory factors, and reprogrammed M2 Phi metabolism. This innovative approach has the potential to reduce breast cancer cell metastasis and enhance sensitivity to chemotherapy drugs such as 6-thioguanine, cisplatin, and doxorubicin (Dox). Mito@ZiF-8 aims to reprogram the M2 Phi microenvironment to support anti-tumor therapies, offering a novel strategy for improving the effectiveness of breast cancer treatment.

With the increased awareness of early tumor detection, the importance of detecting and diagnosing esophageal cancer in its early stages has been underscored. Studies have consistently demonstrated the crucial role of methylation levels in circulating cell-free DNA (cfDNA) in identifying and diagnosing early-stage cancer. cfDNA methylation pertains to the methylation state within the genomic scope of cfDNA and is strongly associated with cancer development and progression. Several research teams have delved into the potential application of cfDNA methylation in identifying early-stage esophageal cancer and have achieved promising outcomes. Recent research supports the high sensitivity and specificity of cfDNA methylation in early esophageal cancer diagnosis, providing a more accurate and efficient approach for early detection and improved clinical management. Accordingly, this review aims to present an overview of methylation-based cfDNA research with a focus on the latest developments in the early detection of esophageal cancer. Additionally, this review summarizes advanced analytical technologies for cfDNA methylation that have significantly benefited from recent advancements in separation and detection techniques, such as methylated DNA immunoprecipitation sequencing (MeDIP-seq). Recent findings suggest that biomarkers based on cfDNA methylation may soon find successful applications in the early detection of esophageal cancer. However, large-scale prospective clinical trials are required to identify the potential of these biomarkers.

BackgroundTo analyze the prognosis and diagnostic value of relevant hematological indexes on the survival status of patients with esophageal squamous cell carcinoma after radical surgery.MethodsThis study included 206 patients with esophageal cancer who underwent surgical R0 resection. The data, including the basic information, preoperative blood routine, albumin, fibrinogen, surgery-related information, postoperative pathology, and overall survival, of the patients were compared.ResultsThe survival and death groups showed a significant difference in overall survival (OS), the degree of differentiation, depth of infiltration, pathological stage, vascular infiltration, nerve infiltration, fibrinogen, white blood cell, neutrophils, platelet, and platelet hematocrit (P<0.05). Tumor located in the middle thorax, larger lesion length, deeper invasion, later pathological stage, vascular infiltration, nerve infiltration, lymph node metastasis, cardiovascular disease, and higher smoking grade were risk factors for poor prognosis of esophageal squamous cell carcinoma (ESCC) (P<0.05). Cardiovascular disease, lower differentiation, tumor located in the middle thorax, and nerve infiltration were independent risk factors for the reduction of survival time of patients with ESCC (P<0.05).ConclusionsHistory of cardiovascular disease, tumor located in the middle chest, poorly differentiated esophageal squamous cell carcinoma, visible nerve cancer invasion, hematocrit (HCT), mean erythrocyte hemoglobin concentration (MCHC), and hemoglobin (HB) are independent risk factors for the long-term survival of patients with ESCC.

Objective: To analyze the optimal timing of lung transplantation and summarize postoperative complications and their management after paraquat poisoning.Methods: Here, we present the clinical course of a 17-year-old boy with paraquat poisoning, in whom bilateral lung transplantation (LT) was performed. We reviewed the eight previously published articles relevant to LT after paraquat poisoning to summarize the therapeutic strategy.Results: A 17-year-old boy was admitted to the hospital after ingestion of 30–50 mL 25% paraquat. Mechanical ventilation was initiated on the 25th day after intoxication. Venovenous extracorporeal membrane oxygenation was initiated on the 26th day. Sequential bilateral LT was performed on the 27th day. Several complex postoperative complications occurred and the patient was discharged on the 50th day postoperatively. Eight case reports were included in the literature review, including 11 patients with paraquat poisoning undergoing LT. Three patients died due to paraquat poisoning leading to fibrosis in the transplanted lungs or postoperative complications. Eight patients survived during follow-up.Conclusion: LT after herbicide poisoning should be planned when hepatorenal function starts to recover, and waiting for complete recovery is unnecessary. Prevention of infection before surgery is important to reduce the incidence of postoperative infection. Complex perioperative complications caused by the herbicide itself or the late timing of transplantation can be successfully managed by a multidisciplinary team.

1 临床资料患者女，16岁，因无诱因出现胸痛2天，加重入院。患者既往身体健康，无传染病、过敏、手术史。实验室检查：血常规、尿常规、肝肾功能未见异常。体格检查：右胸中下部触觉语颤消失。右胸中下部叩诊为实音、听诊呼吸音消失。胸部增强CT:右前纵隔见团块影，边缘轻度强化，大小约11.8 cm×7.8 cm, 以液性成分为主，边缘局部见少许脂肪样低密度影，其内实性结节，大小约1.7 cm×1.3 cm,

Background: The aim of this study was to develop a nomogram model in combination with thromboelastography (TEG) to predict the development of venous thromboembolism (VTE) after lung cancer surgery.Methods: The data of 502 patients who underwent surgical treatment for lung cancer from December 2020 to December 2022 were retrospectively analyzed. Patients were then randomized into training and validation groups. Univariate and multivariate logistic regression analyses were carried out in the training group and independent risk factors were included in the nomogram to construct risk prediction models. The predictive capability of the model was assessed by the consistency index (C-index), receiver operating characteristic curves (ROC), the calibration plot and decision curve analysis (DCA).Results: The nomogram risk prediction model comprised of the following five independent risk factors: age, operation time, forced expiratory volume in one second and postoperative TEG parameters k value(K) and reaction time(R). The nomogram model demonstrated better predictive power than the modified Caprini model, with the C-index being greater. The calibration curve verified the consistency of nomogram between the two groups. Furthermore, DCA demonstrated the clinical value and potential for practical application of the nomogram.Conclusion: This study is the first to combine TEG and clinical risk factors to construct a nomogram to predict the occurrence of VTE in patients after lung cancer surgery. This model provides a simple and user-friendly method to assess the probability of VTE in postoperative lung cancer patients, enabling clinicians to develop individualized preventive anticoagulation strategies to reduce the incidence of such complications.

Objective: This study aims to explore the clinical application of an AI-3D reconstruction system in measuring lung volume and analyze its practical value in donor-recipient size matching in lung transplantation. Methods: The study retrospectively collected data from 75 subjects who underwent a plethysmography examination and lung CT at the First Hospital of Jilin University. General data and information related to lung function, and imaging results were collected. The correlation between actual total lung volume (aTLV), predicted total lung volume (pTLV), and artificial intelligence three-dimensional reconstruction CT lung volume (AI-3DCTVol) was analyzed for the overall, male, and female groups. The correlation coefficient and the absolute error percentage with pTLV and AI-3DCTVol were obtained. Results: In the overall, male, and female groups, there were statistical differences (p <0.05) between the pTLV formula and AI-3D reconstruction compared to the plethysmography examination value. The ICC between pTLV and aTLV for all study participants was 0.788 (95% CI: 0.515-0.893), p <0.001. Additionally, the ICC value between AI-3D reconstruction and aTLV was 0.792 (95% CI: 0.681-0.866), p <0.001. For male study participants, the ICC between pTLV and aTLV was 0.330 (95% CI: 0.032-0.617), p = 0.006. Similarly, the ICC value between AI-3D reconstruction and aTLV was 0.413 (95% CI: 0.089-0.662), p = 0.007. In the case of female research subjects, the ICC between pTLV and aTLV was 0.279 (95% CI: 0.001-0.523), p = 0.012. Further, the ICC value between AI-3D reconstruction and aTLV was 0.615 (95% CI: 0.561-0.870), p <0.001. Conclusion: The AI-3D reconstruction, as a convenient method, has significant potential for application in lung transplantation.

Lung cancer has become one of the key life-threatening factors and is the most common type of tumor. With the improvement of equipment and the improvement of lung cancer awareness, the surgical treatment of lung cancer is becoming more and more mature. Surgery can provide an important part of individualized treatment strategies for patients with different stages of lung cancer and different wishes. In addition, the concept of minimally invasive, precise, and intelligent has triggered a revolutionary change in the surgical treatment strategy for lung cancer. Therefore, this review focuses on the development of lung cancer surgery history, summarizing the era from traditional surgery to the era of minimally invasive thoracic surgery based on TV-assisted thoracic surgery. The operating methods and treatment effects of different surgical methods are comprehensively introduced, and the optimization and improvement of different surgical methods in the future are also discussed. Along with the concept of minimally invasive surgical techniques, there are more and more explorations of nanotechnology in the surgical treatment of lung cancer. The application of nanotechnology in lung cancer imaging, and the combination of surgery with nanomedicine is an effective solution for cancer treatment today. So, this review also summarizes the application prospects of nanotechnology before, during and after lung cancer surgery.

We investigated the clinical therapeutic effects and prognosis of video-assisted thoracoscopic surgery (VATS) in mediastinal lymph node dissection of lung carcinoma. A total of 312 patients were divided into high-risk and conventional risk groups according to the severity of the disease. High-risk group (n=137) received thoracoscope-guided anatomical pulmonary segmentectomy and systematic lymph node dissection as well as conventional risk group (n=175) received thoracoscope-guided pulmonary lobectomy and systematic lymph node dissection. The results revealed that there are significant differences in age, gender, location, lymph node resection methods, and histological classification in the two groups (P<0.05). Moreover, in comparison with the high-risk group, T stage was higher in the conventional group and showed significant statistical significance (P<0.01). The analysis of independent risk factors of the above differences showed that T staging and histological classification showed high-risk coefficients for lymph node dissection. The risk coefficient was increased with patients' age. The 5-year survival rate, disease-free survival, and postoperative recurrence rate of the patients in the two groups all indicated no obvious statistical differences. Consequently, thoracoscope-guided lymph node dissection could enhance the detection rate of lymph node metastasis. For the adenocarcinoma (AD) patients with T staging greater than T1, lymph node dissection could provide more accurate pathological staging. Anatomical pulmonary segmentectomy combined with systematic lymph node dissection should be applied in the treatment of elderly, high-risk, and advanced stage (prothrombin time (PT) state >2 cm, ≤3 cm) patients with non-small cell lung carcinoma (NSCLC). Taken together,thoracoscope-guided lymph node dissection could improve the detection rate of lymph node metastasis. In this case, the complete resection of lesions could be ensured. Besides, normal pulmonary tissues were preserved to the maximum extent with minimal trauma, safety, fast postoperative recovery, and definite long-term therapeutic effects.

Immune checkpoint blockade therapy is an important advance in cancer treatment, and the representative drugs (PD-1/PD-L1 antibodies) have greatly improved clinical outcomes in various human cancers. However, since many patients still experience primary resistance, they do not respond to anti-PD1/PD-L1 therapy, and some responders also develop acquired resistance after an initial response. Therefore, combined therapy with anti-PD-1/PD-L1 immunotherapy may result in better efficacy than monotherapy. In tumorigenesis and tumor development processes, the mutual regulation of autophagy and tumor immune escape is an intrinsic factor of malignant tumor progression. Understanding the correlation between the tumor autophagy pathway and tumor immune escape may help identify new clinical cancer treatment strategies. Since both autophagy and immune escape of tumor cells occur in a relatively complex microenvironmental network, autophagy affects the immune-mediated killing of tumor cells and immune escape. Therefore, comprehensive treatment targeting autophagy and immune escape to achieve “immune normalization” may be an important direction for future research and development. The PD-1/PD-L1 pathway is essential in tumor immunotherapy. High expression of PD-L1 in different tumors is closely related to poor survival rates, prognoses, and treatment effects. Therefore, exploring the mechanism of PD-L1 expression is crucial to improve the efficacy of tumor immunotherapy. Here, we summarize the mechanism and mutual relationship between autophagy and PD-L1 in antitumor therapy, which may help enhance current antitumor immunotherapy approaches.

Objective: The objective of this study is to determine the drug resistance status of pulmonary tuberculosis patients in Jilin Province.Methods: A retrospective survey was conducted on 395 sputum culture TB-positive patients admitted to the tuberculosis hospital in Jilin Province in 2019. Sputum samples were cultured in acidic Roche medium. Drug sensitivity testing was conducted using the proportional method. Sensitivity was reported if the percentage of drug resistance was less than 1%, and resistance was reported if the percentage was ≥1%. Statistical analysis was performed using SPSS 22.0.Results: 395 tuberculosis patients with positive sputum tuberculosis culture were included in the study, with 102 being initially treated and 293 being retreated. The study population consisted of 283 males and 112 females. Sex, age, nationality, occupation, marital status, diabetes comorbidity, initial treatment, normal health status, BCG vaccine vaccination, smoking, and alcohol consumption were considered as factors that may affect the rate of multidrug resistance. And only the history of treatment (initial treatment) was associated with multidrug resistance (p = 0.032). This indicates that retreatment is the most significant risk factor for the occurrence of multidrug resistance in tuberculosis. The multidrug resistance rate in retreated patients is 3.764 times higher than that in initially treated patients.Conclusion: The prevalence of multidrug-resistant is higher in retreated patients compared to initially treated patients in the study population. Multidrug resistance is only associated with the treatment history (initial retreatment) and not with other factors.

Lung cancer is a widely occurring and deadly malignancy, with high prevalence rates in China and across the globe. Specifically, non-small cell lung cancer (NSCLC) represents about 85% of all lung cancer cases. The 5-year disease-free survival rate after surgery for stage IB-IIIB NSCLC patients (disease-free survival, DFS) has notably declined from 73% to 13%. Early detection of abnormal cancer molecules and subsequent personalized treatment plans are the most effective ways to address this problem. Liquid biopsy, surprisingly, enables safe, accurate, non-invasive, and dynamic tracking of disease progression. Among the various modalities, circulating tumor DNA (ctDNA) is the most commonly used liquid biopsy modality. ctDNA serves as a credible "liquid biopsy" diagnostic tool that, to a certain extent, overcomes tumor heterogeneity and harbors genetic mutations in malignancies, thereby providing early information on tumor genetic alterations. Despite considerable academic interest in the clinical significance of ctDNA, consensus on its utility remains lacking. In this review, we assess the role of ctDNA testing in the diagnosis and management of NSCLC as a reference for clinical intervention in this disease. Lastly, we examine future directions to optimize ctDNA for personalized therapy.